The document discusses gas exchange and respiratory failure. It defines two types of respiratory failure: hypoxemic and hypercapnic. Hypoxemic respiratory failure occurs when there is inadequate oxygen transfer, while hypercapnic respiratory failure occurs when there is insufficient carbon dioxide removal. The major mechanisms that can cause hypoxemic respiratory failure are ventilation-perfusion mismatching, shunting of blood, diffusion limitation across the alveolar-capillary membrane, and alveolar hypoventilation. Common diseases associated with each type of respiratory failure are also outlined.

1. Mrs Dipali Dumbre
M.Sc. Nursing
Medical Surgical Nursing
SCON

2. GAS EXCHANGE
 The major function of the respiratory system is gas
exchange, which involves the transfer of oxygen (O2) and
carbon dioxide (CO2) between the atmosphere and the
blood.

3.  Insufficient O2 is transferred to the blood or
inadequate CO2 is removed from the lungs.
 Clinical states that interfere with adequate O2 transfer
result in hypoxemia, which is manifested by a
decrease in arterial O2 tension (PaO2) and saturation
(SaO2).
 Insufficient CO2 removal results in hypercapnia,
which is manifested by an increase in arterial CO2
tension (PaCO2).

4.  Respiratory failure is not a disease; it is a condition that
occurs as a result of one or more diseases involving the
lungs or other body systems.
 Respiratory failure can be classified as
 Hypoxemic
 Hypercapnic .

5.  Hypoxemic respiratory failure is also referred to as
oxygenation failure because the primary problem is
inadequate O2 transfer between the alveoli and the
pulmonary capillary bed.
 Hypoxemic respiratory failure is commonly defined as
a PaO2 of 60 mm Hg or less when the patient is receiving
an inspired O2 concentration of 60% or greater.
This definition incorporates two important concepts:
 The PaO2 is at a level that indicates inadequate O2
saturation of hemoglobin.
 This PaO2 level exists despite administration of
supplemental O2 at a percentage (60%)

6.  Disorders that interfere with O2 transfer into the blood
include
 Pneumonia,
 Pulmonary edema,
 Pulmonary emboli,
 Alveolar injury related to inhalation of toxic gases (e.g.,
smoke), as well as lung damage related to alveolar
stress/ventilator-induced lung injury.
 In addition, low cardiac output states (e.g., heart failure,
shock) can also cause hypoxemic respiratory failure

7.  Hypercapnic respiratory failure is also referred to as
ventilatory failure because the primary problem is
insufficient CO2 removal.
 Hypercapnic respiratory failure is commonly defined
as a PaCO2 above normal (greater than 45 mm Hg) in
combination with acidemia (arterial pH less than 7.35).
This definition incorporates three important concepts:
 The PaCO2 is higher than normal.
 There is evidence of the body's inability to compensate for
this increase (acidemia)
 The pH is at a level where a further decrease may lead to
severe acid-base imbalance.

8.  Disorders that compromise lung ventilation and
subsequent CO2 removal include drug overdoses with
central nervous system (CNS) depressants, neuromuscular
diseases (e.g., myasthenia gravis), and trauma or diseases
involving the spinal cord and its role in lung ventilation.
 Acute asthma is also associated with hypercapnic
respiratory failure. Many patients experience both
hypoxemic and hypercapnic respiratory failure.

9. CAUSES
HYPOXEMIC RESPIRATORY FAILURE HYPERCAPNIC RESPIRATORY
FAILURE
Respiratory System
Asthma
COPD
Pneumonia
Cystic fibrosis
Toxic inhalation
Asthma
COPD
Cystic fibrosis
Cardiac System
Morbid obesity
Anatomic shunt (e.g., ventricular septal
defect)
Neuromuscular System
Cardiogenic pulmonary edema
Myasthenia gravis
Critical illness polyneuropathy
Acute myopathy
Toxic ingestion (e.g., tree tobacco)
Guillain-Barré syndrome
Poliomyelitis
Muscular dystrophy
Multiple sclerosis

10. CENTRAL NERVOUS SYSTEM
Hepatopulmonary syndrome
Brainstem injury/infarction
Sedative and opioid overdose
Spinal cord injury
Massive pulmonary embolism (e.g., thrombus
emboli, fat emboli)
Severe head injury
Chest Wall
Pulmonary artery laceration and hemorrhage
Thoracic trauma (e.g., flail chest)

11. Classification of respiratory failure.

12. Pathophysiology
Hypoxemic Respiratory Failure
 Four physiologic mechanisms may cause hypoxemia and
subsequent hypoxemic respiratory failure:
1. Mismatch between ventilation (V) and perfusion
(Q),(V/Q)
2. Shunt;
3. Diffusion limitation
4. Hypoventilation.
The most common causes are V/Q mismatch and shunt.

13. Ventilation-Perfusion (V/Q) Mismatch
 In the normal lung, the volume of blood perfusing the
lungs each minute (4 to 5 L) is approximately equal to the
amount of fresh gas that reaches the alveoli each minute
(4 to 5 L).
 In a perfectly matched system, each portion of the lung
would receive about 1 ml of air for each 1 ml of blood flow.
 This match of ventilation and perfusion would result in a
V/Q ratio of 1:1 (e.g., 1 ml of air per 1 ml of blood), which is
expressed as V/Q = 1.
 Ventilation is ideally matched with perfusion.

14.  Although this example implies that ventilation and
perfusion are ideally matched in all areas of the lung.
But this situation does not normally exist.
 In reality, there is some regional mismatch.
 At the lung apex, V/Q ratios are greater than 1 (more
ventilation than perfusion).
 At the lung base, V/Q ratios are less than 1 (less
ventilation than perfusion).
 Because changes at the lung apex balance changes at the
base, the net effect is a close overall match

15.  Regional V/Q differences in the normal lung. At the lung
apex, the V/Q ratio is 3.3, at the midpoint 1.0, and at the
base 0.63. This difference causes the PaO2 to be higher at
the apex of the lung and lower at the base. Values for
PaCO2 are the opposite (i.e., lower at the apex and higher at
the base). Blood that exits the lung is a mixture of these
values.

16.  Many diseases and conditions alter overall V/Q matching
and thus cause V/Q mismatch.
 The most common are those in which increased
secretions are present in the airways (e.g., chronic
obstructive pulmonary disease [COPD]) or alveoli (e.g.,
pneumonia), and when bronchospasm is present (e.g.,
asthma).
 V/Q mismatch may also result from alveolar collapse
(atelectasis) or as a result of pain.
 Unrelieved or inadequately relieved pain interferes with
chest and abdominal wall movement, compromising lung
ventilation.
 Additionally, pain increases muscle and motor tension,
producing generalized muscle rigidity; causes systemic
vasoconstriction and activation of the stress response; and
increases O2 consumption and CO2 production

17.  In this circumstance, increased metabolic (oxygen)
demand and CO2 production increase the demand side
of the equation and may increase both oxygen and
ventilation demands.
 All of these conditions result in limited airflow
(ventilation) to alveoli but have no effect on blood flow
(perfusion) to the gas exchange units.
 The consequence is V/Q mismatch.
 A pulmonary embolus affects the perfusion portion of
the V/Q relationship.
 The embolus limits blood flow but has no effect on
airflow to the alveoli, again causing V/Q mismatch.

18.  Range of ventilation to perfusion (V/Q) relationships. A, Absolute shunt, no
ventilation due to fluid filling the alveoli. B, V/Q mismatch, ventilation
partially compromised by secretions in the airway. C, Normal lung unit. D,
V/Q mismatch, perfusion partially compromised by emboli obstructing
blood flow. E, Dead space, no perfusion due to obstruction of the pulmonary
capillary.

19.  O2 therapy is an appropriate first step to reverse
hypoxemia caused by V/Q mismatch because not all
gas exchange units are affected.
 O2 therapy increases the PaO2 in blood leaving
normal gas exchange units, thus causing a higher than
normal PaO2.
 The well-oxygenated blood mixes with poorly
oxygenated blood, raising the overall PaO2 of blood
leaving the lungs.

20. Shunt.
 Shunt occurs when blood exits the heart without having
participated in gas exchange.
 A shunt can be viewed as an extreme V/Q mismatch .
There are two types of shunt:
 Anatomic and Intrapulmonary.
 An anatomic shunt occurs when blood passes through an
anatomic channel in the heart (e.g., a ventricular septal
defect) and therefore does not pass through the lungs.
 An intrapulmonary shunt occurs when blood flows
through the pulmonary capillaries without participating in
gas exchange.
 Intrapulmonary shunt is seen in conditions in which the
alveoli fill with fluid (e.g., acute respiratory distress
syndrome [ARDS], pneumonia, pulmonary edema).

21.  O2 therapy alone may be ineffective in increasing the PaO2
if hypoxemia is due to shunt because
 Blood passes from the right to the left side of the heart
without passing through the lungs (anatomic shunt);
or
 The alveoli are filled with fluid, which prevents gas
exchange (intrapulmonary shunt).
 Patients with shunt are usually more hypoxemic than
patients with V/Q mismatch, and they may require
mechanical ventilation and a high fraction of inspired
oxygen (FIO2) to improve gas exchange.

22. Diffusion Limitation
 Diffusion limitation occurs when gas exchange across
the alveolar-capillary membrane is compromised by a
process that thickens or destroys the membrane .
 Diffusion limitation can also be worsened by conditions
that affect the pulmonary vascular bed such as severe
emphysema or recurrent pulmonary emboli.
 Some diseases cause the alveolar-capillary membrane to
become thicker (fibrotic), which slows gas transport.
 These diseases include pulmonary fibrosis, interstitial lung
disease, and ARDS.

23.  Diffusion limitation is more likely to cause hypoxemia
during exercise than at rest.
 During exercise, blood moves more rapidly through the
lungs. Because transit time is increased, red blood cells are
in the lungs for a shorter time, decreasing the time for
diffusion of O2 across the alveolar-capillary membrane.
 The classic sign of diffusion limitation is hypoxemia that is
present during exercise but not at rest.

25. Alveolar Hypoventilation
 Alveolar hypoventilation is a generalized decrease in
ventilation that results in an increase in the PaCO2 and a
consequent decrease in PaO2.
 Alveolar hypoventilation may be the result of restrictive
lung diseases, CNS diseases, chest wall dysfunction, acute
asthma, or neuromuscular diseases.
 Although alveolar hypoventilation is primarily a
mechanism of hypercapnic respiratory failure, it is
mentioned here because it can also cause hypoxemia.

26. Interrelationship of Mechanisms
 Frequently, hypoxemic respiratory failure is caused by a
combination of two or more of the following:
 V/Q mismatch, shunting, diffusion limitation, and
hypoventilation.
 The patient with acute respiratory failure secondary to
pneumonia may have a combination of V/Q mismatch and
shunt because the inflammation, edema, and hypersecretion
of exudate within the bronchioles and terminal respiratory
units obstruct the airways (V/Q mismatch) and fill the alveoli
with exudate (shunt).
 In addition, shunt may be increased because of improper
positioning (e.g., bad lung down) and endogenous vasodilator
mediators as is the case with pneumococcal pneumonia.
 The patient with cardiogenic pulmonary edema or ARDS may
have a combination of shunt and V/Q mismatch because some
alveoli are completely filled with fluid from edema (shunt) and
others are partially filled with fluid (V/Q mismatch).

27. Hypercapnic Respiratory Failure

28.  Hypercapnic respiratory failure results from an imbalance
between ventilatory supply and ventilatory demand.
 Ventilatory supply is the maximum ventilation (gas flow in
and out of the lungs) that the patient can sustain without
developing respiratory muscle fatigue.
 Ventilatory demand is the amount of ventilation needed to
keep the PaCO2 within normal limits.
 Normally, ventilatory supply far exceeds ventilatory
demand. As a consequence, individuals with normal lung
function can engage in strenuous exercise, which greatly
increases CO2 production without an elevation in PaCO2.
 Patients with preexisting lung disease such as severe
COPD do not have this advantage and cannot effectively
increase lung ventilation in response to exercise or
metabolic demands.
 However, considerable dysfunction is typically present
before ventilatory demand exceeds ventilatory supply.

29.  When ventilatory demand does exceed ventilatory supply,
the PaCO2 can no longer be sustained within normal limits
and hypercapnia occurs.
 Hypercapnia reflects substantial lung dysfunction.
Hypercapnic respiratory failure is sometimes called
ventilatory failure because the primary problem is the
inability of the respiratory system to ventilate out sufficient
CO2 to maintain a normal PaCO2.
 Hypercapnic respiratory failure can also be differentiated
as acute or chronic respiratory failure.
 For example, an episode of respiratory failure may
represent an acute decompensation in a patient whose
underlying lung function has deteriorated to the point that
some degree of decompensation is always present (chronic
respiratory insufficiency).

30. Pathophysiology
(1) Abnormalities of the airways and alveoli,
(2) Abnormalities of the CNS
(3) Abnormalities of the chest wall
(4) Neuromuscular conditions.

31. Airways and Alveoli
 Patients with asthma, COPD, and cystic fibrosis are at high
risk for hypercapnic respiratory failure because the
underlying pathophysiology of these conditions results in
airflow obstruction and air trapping

32. Central Nervous System
 A variety of problems may suppress the drive to breathe.
 A common example is an overdose of an opioid or other
respiratory depressant drug.
 In a dose-related manner, CNS depressants such as
opioids and benzodiazepines decrease CO2 reactivity in
the brainstem, allowing arterial CO2 levels to rise.
 A brainstem infarction or severe head injury may also
interfere with normal function of the respiratory center in
the medulla.
 Patients with these conditions are at risk for respiratory
failure because the medulla does not alter the respiratory
rate in response to a change in PaCO2.

33.  Independent of direct brainstem dysfunction,
metabolic or structural brain injury resulting in
significant depression of consciousness or loss of
consciousness may interfere with the patient's ability
to manage secretions or adequately protect his or her
airway.
 CNS dysfunction may also include high-level spinal
cord injuries that limit innervation to the respiratory
muscles of the chest wall and diaphragm.

34. Chest Wall
 A variety of conditions may prevent normal movement of
the chest wall and hence limit lung expansion.
 In patients with flail chest, fractures prevent the rib cage
from expanding normally because of pain, mechanical
restriction, and muscle spasm.
 In patients with kyphoscoliosis, the change in spinal
configuration compresses the lungs and prevents normal
expansion of the chest wall.
 In patients with morbid obesity, the weight of the chest
and abdominal contents may limit lung expansion.
 Patients with these conditions are at risk for respiratory
failure because these dysfunctions limit lung expansion or
diaphragmatic movement and consequently gas exchange.

35. Neuromuscular Conditions
 Various types of neuromuscular diseases may result in
respiratory muscle weakness or paralysis .
 For example, patients with Guillain-Barré syndrome,
muscular dystrophy, myasthenia gravis (acute
exacerbation), or multiple sclerosis are at risk for
respiratory failure because the respiratory muscles are
weakened or paralyzed as a consequence of the
underlying neuromuscular condition.
 Therefore they are unable to maintain normal PaCO2
levels.

36. Tissue Oxygen Needs
 It is important to remember that even though PaO2 and
PaCO2 determine the definition of respiratory failure,
 the major threat of respiratory failure is the inability of
the lungs to meet the oxygen demands of the tissues.
 This inability may occur as a result of inadequate tissue O2
delivery or because the tissues are unable to use the O2
delivered to them.
 It may also occur as a result of the stress response and
dramatic increases in tissue oxygen consumption.
 Tissue O2 delivery is determined by the amount of O2
carried in the hemoglobin, as well as cardiac output

37.  Therefore respiratory failure places the patient at greater
risk if there are coexisting cardiac problems or anemia.
 Failure of O2 utilization most commonly occurs as a result
of septic shock.
 n this situation, adequate O2 may be delivered to the body
tissues, but due to impaired oxygen extraction, an
abnormally high amount of O2 returns in the venous
blood because it is not used or off-loaded at the tissue
level.
 Acid-base alterations (e.g., alkalosis, acidosis) may also
interfere with oxygen delivery to peripheral tissues.

38. CLINICAL MANIFESTATION

39.  Respiratory failure may develop suddenly (minutes or
hours) or gradually (several days or longer).
 A sudden decrease in PaO2 or a rapid rise in PaCO2 implies
a serious condition, which can rapidly become a life-
threatening emergency.
 An example is the patient with asthma who develops severe
bronchospasm and a marked decrease in airflow, resulting
in respiratory arrest.
 A more gradual change in PaO2 and PaCO2 is better
tolerated because compensation can occur.
 An example is the patient with COPD who develops a
progressive increase in PaCO2 over several days following
the onset of a respiratory infection.
 Because the change occurred over several days, there is
time for renal compensation (e.g., retention of
bicarbonate), which will minimize the change in arterial
pH. The patient will have compensated respiratory acidosis

40.  Manifestations of respiratory failure are related to the
extent of change in PaO2 or PaCO2, the rapidity of change
(acute versus chronic), and the ability to compensate to
overcome this change.
 When the patient's compensatory mechanisms fail,
respiratory failure occurs.
 the initial indication of respiratory failure is a change in
the patient's mental status. Because the cerebral cortex is
so sensitive to variations in oxygenation, arterial CO2
levels, and acid-base balance, mental status changes will
occur early and frequently before ABG results are
obtained.
 Restlessness, confusion, agitation, and combative
behavior suggest inadequate delivery of O2 to the brain
and should be fully investigated

41.  The manifestations of respiratory failure are specific (arise
from the respiratory system) AND nonspecific (arise from
other body systems)
 An understanding of the significance of these
manifestations is critical to the ability to detect the onset
of respiratory failure and effectiveness of treatment.
 Tachycardia and mild hypertension can also be early signs
of respiratory failure.
 Such changes may indicate an attempt by the heart to
compensate for decreased O2 delivery.
 A severe morning headache may suggest that hypercapnia
may have occurred during the night, increasing cerebral
blood flow by vasodilation and causing a morning
headache.

42.  At night the respiratory rate is slower and the lungs of
patients at risk for respiratory failure may remove less
PaCO2.
 Rapid, shallow breaths suggest that the tidal volume may
be inadequate to remove CO2 from the lungs.
 Cyanosis is an unreliable indicator of hypoxemia and is a
late sign of respiratory failure because it does not occur
until hypoxemia is severe (PaO2 #45 mm Hg).

43. Hypoxemic C/M
SPECIFIC NONSPECIFIC
Respiratory
Dyspnea
Tachypnea
Prolonged expiration
(I:E 1:3, 1:4)
Intercostal muscle retraction
Use of accessory muscles in respiration
↓ SpO2 (<80%)
Paradoxic chest/abdominal wall
movement with respiratory cycle (late)
Cyanosis (late)
Cerebral
Agitation
Disorientation
Delirium
Restless, combative behavior
Confusion
↓ Level of consciousness
Coma (late)
Cardiac
Tachycardia
Hypertension
Skin cool, clammy, and diaphoretic
Dysrhythmias (late)
Hypotension (late)

44. Hypercapnia C/M
SPECIFIC NONSPECIFIC
Respiratory
Dyspnea
↓ Respiratory rate or ↑ rapid rate with
shallow respirations
↓ Tidal volume
↓ Minute ventilation
Cerebral
Morning headache
Disorientation
Progressive somnolence
Coma (late)
Cardiac
Dysrhythmias
Hypertension
Tachycardia
Bounding pulse
Neuromuscular
Muscle weakness
↓ Deep tendon reflexes
Tremor, seizures (late)
Other
Pursed-lip breathing
Use of tripod position

45. Specific Clinical Manifestations
 The patient in respiratory failure may have several clinical
findings indicating distress.
 The patient may have a rapid, shallow breathing pattern or
a respiratory rate that is slower than normal.
 Both changes predispose to insufficient CO2 removal. The
patient may increase the respiratory rate in an effort to
blow off accumulated CO2.
 This breathing pattern requires a substantial amount of
work and predisposes to respiratory muscle fatigue.
 A change from a rapid rate to a slower rate in a patient in
acute respiratory distress such as that seen with acute
asthma suggests extreme progression of respiratory muscle
fatigue and increased probability of respiratory arrest

46.  The position that the patient assumes is an indication of the
effort associated with breathing.
 The patient may be able to lie down (mild distress), be able to
lie down but prefer to sit (moderate distress), or be unable to
breathe unless sitting upright (severe distress).
 A common position is to sit with the arms propped on the
overbed table.
 This position, called the tripod position, helps decrease the
work of breathing because propping the arms increases the
anterior-posterior diameter of the chest and changes pressure in
the thorax. Pursed-lip breathing may be used.
 This strategy causes an increase in SaO2 because it slows
respirations, allows more time for expiration, and prevents the
small bronchioles from collapsing, thus facilitating air
exchange.
 Another assessment parameter is the number of pillows the
patient requires to breathe comfortably when attempting to lie
flat.
 This is termed orthopnea and may be documented as one-, two-
, three-, or four-pillow orthopnea.

47.  The person who is experiencing dyspnea is working hard
to breathe and may be able to speak only a few words at a
time between breaths.
 The ability of the patient to speak without pausing to
breathe is an indication of the severity of dyspnea.
 The patient may speak in sentences (mild or no distress),
phrases (moderate distress), or words (severe distress).
 The number of words is also a clue (e.g., how many words
can the patient say without pausing to breathe?).
 The patient may have “two-word” or “three-word”
dyspnea, signifying that only two or three words can be
said before pausing to breathe.
 There may also be earlier onset of fatigue with walking. An
additional assessment parameter is how far the patient is
able to walk without stopping to rest.

48.  There may be a change in the inspiratory (I) to expiratory (E)
(I:E) ratio.
 Normally, the I:E ratio is 1:2, which means that expiration is
twice as long as inspiration.
 In patients in respiratory distress, the ratio may increase to 1:3
or 1:4.
 This change signifies airflow obstruction and that more time is
required to empty the lungs.
 Retraction (inward movement) of the intercostal spaces or the
supraclavicular area and use of the accessory muscles (e.g.,
sternocleidomastoid) during inspiration or expiration. Use of
the accessory muscles signifies moderate distress.
 Paradoxic breathing indicates severe distress. Normally, the
thorax and abdomen move outward on inspiration and inward
on exhalation.
 During paradoxic breathing, the abdomen and chest move in
the opposite manner—outward during exhalation and inward
during inspiration.

49.  Paradoxic breathing results from maximal use of the accessory
muscles of respiration. The patient may also be diaphoretic
from the work associated with breathing.
 Auscultation should be performed in order to assess the
patient's baseline breath sounds, as well as any changes from
baseline.
 The nurse should note the presence and location of any
adventitious breath sounds.
 Crackles may indicate pulmonary edema and rhonchi may
indicate COPD.
 Absent or diminished breath sounds may indicate atelectasis or
pleural effusion.
 The presence of bronchial breath sounds over the lung
periphery often results from lung consolidation that is seen
with pneumonia.
 A pleural friction rub may also be heard in the presence of
pneumonia that has involved the pleura.

50. Diagnostic Studies
 History and physical examination
 Arterial blood gases
 Pulse oximetry
 Chest x-ray
 CBC
 Serum electrolytes and urinalysis
 ECG
 Blood and sputum cultures

51. Collaborative Therapy

52. Respiratory Therapy
 The major goals of care for acute respiratory failure
include maintaining adequate oxygenation and
ventilation.
 This goal is accomplished by collaboration among the
nursing, medical, and respiratory care teams.
 The interventions used include
 O2 therapy,
 Mobilization of secretions,
 Positive pressure ventilation (PPV)

53. O2 therapy
 The primary goal of O2 therapy is to correct hypoxemia.
 If hypoxemia is secondary to V/Q mismatch,
supplemental O2 administered at 1 to 3 L/min by nasal
cannula or 24% to 32% by simple face mask or Venturi
mask should improve the PaO2, SaO2, and SpO2.
 Hypoxemia secondary to an intrapulmonary shunt is
usually not responsive to high O2 concentrations, and the
patient will usually require PPV.

54.  The type of O2 delivery system chosen for the patient in
acute respiratory failure should
 (1) be tolerated by the patient, because anxiety caused by
feelings of claustrophobia related to the face mask or
dyspnea may prompt the patient to remove the O2 device.
 (2) maintain PaO2 at 55 to 60 mm Hg or more and SaO2 at
90% or more at the lowest O2 concentration possible.
 High O2 concentrations replace the nitrogen gas normally
present in the alveoli, causing instability and atelectasis.

55. Mobilization of Secretions.
 Retained pulmonary secretions may cause or exacerbate
acute respiratory failure by blocking movement of O2 into
the alveoli and pulmonary capillary blood and removal of
CO2 during the respiratory cycle.
 Secretions can be mobilized through effective coughing,
adequate hydration and humidification, chest physical
therapy (chest physiotherapy), and tracheal suctioning.

56. Effective Coughing and Positioning.
 If secretions are obstructing the airway, the patient should be
encouraged to cough.
 The patient with a neuromuscular weakness from a disease or
exhaustion may not be able to generate sufficient airway
pressures to produce an effective cough.
 Augmented coughing (quad coughing) may be of benefit to
these patients.
 Augmented coughing is performed by placing the palm of the
hand (or the palms of both hands) on the abdomen below the
xiphoid process
 As the patient ends a deep inspiration and begins the
expiration, the hands should be moved forcefully downward,
increasing abdominal pressure and facilitating the cough.
 This measure helps increase expiratory flow and thereby
facilitates secretion clearance.

58.  Some patients may benefit from therapeutic cough
techniques.
 Huff coughing is a series of coughs performed while saying
the word “huff.” This technique prevents the glottis from
closing during the cough.
 Patients with COPD generate higher flow rates with a huff
cough than is possible with a normal cough.
 The huff cough is effective in clearing only the central
airways, but it may assist in moving secretions upward.
 The staged cough also assists secretion mobilization. To
perform the staged cough, the patient sits in a chair,
breathes three or four times in and out through the mouth,
and coughs while bending forward and pressing a pillow
inward against the diaphragm.

59.  Positioning the patient either by elevating the head of the
bed at least 45 degrees or by using a reclining chair or
chair bed may help maximize thoracic expansion, thereby
decreasing dyspnea and improving secretion
mobilization.
 A sitting position improves pulmonary function and
assists in venous pooling in dependent body areas such as
the lower extremities.
 When lungs are upright, ventilation and perfusion are
best in the lung bases.
 Lateral or side-lying positioning may be used in patients
with disease involving only one lung.
 This position, termed good lung down, allows for
improved V/Q matching in the affected lung.
 Pulmonary blood flow and ventilation are optimal in
dependent lung areas.

60.  This positioning also allows for secretions to drain out of
the affected lung to the point where they may be removed
by suctioning.
 For example, in patients with significant right-sided
pneumonia, optimal positioning would be to place them
on their left side to maximize ventilation and perfusion in
the “good” lung and facilitate secretion removal from the
affected lung (postural drainage).
 All patients should be side-lying if there is any possibility
that the tongue will obstruct the airway or that aspiration
may occur.
 An oral or nasal airway should be kept at the bedside for
use if necessary.

61. Hydration and Humidification
 Thick and viscous secretions are difficult to move and
should be thinned.
 Adequate fluid intake (2 to 3 L/day) is necessary to keep
secretions thin and easy to expel.
 If the patient is unable to take sufficient fluids orally,
intravenous (IV) hydration will be used.
 Thorough assessment of the patient's cardiac and renal
status is essential to determine whether he or she can
tolerate the intravascular volume and avoid heart failure
and pulmonary edema.
 Assessment for signs of fluid overload (e.g., crackles,
dyspnea, increased central venous pressure) at regular
intervals is also essential.
 These considerations would also apply to the patient with
renal dysfunction.

62. Chest Physical Therapy
 Chest physical therapy is indicated in patients who
produce more than 30 ml of sputum per day or have
evidence of severe atelectasis or pulmonary infiltrates.
 If tolerated, postural drainage, percussion, and vibration
to the affected lung segments may assist in moving
secretions to the larger airways where they may be
removed by coughing or suctioning.
 Because positioning may affect oxygenation, patients may
not tolerate head-down or lateral positioning because of
extreme dyspnea or hypoxemia caused by V/Q mismatch.

63. Airway Suctioning
 If the patient is unable to expectorate secretions, nasopharyngeal,
oropharyngeal, or nasotracheal suctioning (blind suctioning without
a tracheal tube in place) is indicated.
 Suctioning through an artificial airway, such as endotracheal or
tracheostomy tubes, may also be performed.
 A mini-tracheostomy (or mini-trach) may be used to suction patients
who have difficulty mobilizing secretions and when blind suctioning
is difficult or ineffective.
 The mini-trach is a 4-mm indwelling plastic cuffless cannula inserted
through the cricothyroid membrane.
 It is used to instill sterile normal saline solution to elicit a cough and
to perform suctioning using a size 10 or less French catheter.
 Contraindications for a mini-trach include an absent gag reflex,
history of aspiration, and the need for long-term mechanical
ventilation.
 At all times, suctioning is done cautiously because it may precipitate
hypoxia.

64. Positive Pressure Ventilation
 If intensive measures fail to improve ventilation and
oxygenation and the patient continues to exhibit
manifestations of acute respiratory failure, ventilatory
assistance may be initiated.
 PPV may be provided invasively through orotracheal or
nasotracheal intubation or noninvasively through a nasal
or face mask.
 Patients who require PPV are typically cared for in a
critical care unit.

65. Drug Therapy
 Relief of Bronchospasm.
 Alveolar ventilation will be increased with relief of
bronchospasm.
 Short-acting bronchodilators, such as metaproterenol are
frequently administered to reverse bronchospasm using
either a handheld nebulizer or a metered-dose inhaler
with a spacer.
 In acute bronchospasm these drugs may be given at 15- to
30-minute intervals until it can be determined that a
response is occurring.

66.  Reduction of Airway Inflammation.
 Corticosteroids may be used in conjunction with
bronchodilating agents when bronchospasm and
inflammation are present.
 When administered IV, corticosteroids have an immediate
onset of action.
 Inhaled corticosteroids are not used for acute respiratory
failure, because they require 4 to 5 days before optimum
therapeutic effects are seen.

67.  Treatment of Pulmonary Infections.
 Pulmonary infections (pneumonia, acute bronchitis) result in
excessive mucus production, fever, increased oxygen
consumption, and inflamed, fluid-filled, or collapsed alveoli.
 Alveoli that are fluid filled or collapsed cannot participate in
gas exchange.
 Pulmonary infections can either cause or exacerbate acute
respiratory failure.
 IV antibiotics, such as vancomycin (Vancocin) or ceftriaxone
(Rocephin), are frequently administered to inhibit bacterial
growth.
 Chest x-rays are performed to determine the location and
extent of a suspected infectious process.
 Sputum cultures are used to determine the type of organisms
causing the infection and their sensitivity to antimicrobial
medications.